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image of Rosuvastatin Reduces Allostatic Overload due to Mechanical Strain: A New Finding on Vascular Remodeling Linked to Hypertension in Spontaneously Hypertensive Rats

Abstract

Introduction

Chronic hemodynamic overload due to hypertension produces cardiovascular remodeling, where mechanical stretch (MS) deformation, neurohumoral factors, and/or chronic interaction promote a harmful allostatic overload. Previously, our laboratory demonstrated that rosuvastatin modulates the NO-Hsp70-WT1 pathway during MS at the renal level, and other authors have reported that some statins inhibit the proliferation of rat vascular smooth muscle cells (VSMC) induced by MS. Therefore, this study aims to evaluate, in VSMC culture, the possible modulation of rosuvastatin on NO-Hsp70-WT1 signaling linked to MS and its impact on vascular remodeling due to hypertension.

Methods

After 10 weeks of age, mesenteric vascular smooth muscle cells (VSMCs) were cultured from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Prior to cell culture, systolic blood pressure (SBP) was measured: SHR exhibited SBP of 180 ± 10 mmHg, while WKY rats had SBP of 125 ± 8 mmHg. Eight experimental groups were established: SHR and WKY, each with or without mechanical stretch (MS) for 48 hours (Flexcell® system), and with or without treatment with rosuvastatin (10−5 mol/L). Apoptosis was assessed by flow cytometry, while fibrosis was evaluated TGF-β levels. Nitric oxide (NO) levels, as well as WT1 and Hsp70 expression, were also analyzed.

Results

SHR cultures without MS vs WKY without MS showed higher apoptosis/fibrosis and low NO, WT1, and Hsp70 ( < 0.01). Notably, WKY with MS was similar to SHR without MS. Furthermore, when comparing SHR with MS vs SHR without MS, we verified more significant apoptosis/fibrosis with lower NO, WT1, and Hsp70 ( < 0.01). However, rosuvastatin reduced these differences, promoting the restoration of the altered parameters.

Discussion

Mechanical Stretch (MS) induces apoptosis and fibrosis in vascular smooth muscle cells (VSMCs) from hypertensive rats, correlating with impaired nitric oxide (NO) production. Rosuvastatin treatment significantly attenuated MS-induced damage and restored NO bioavailability. Critically, MS downregulated the expression of WT1 and Hsp70, and rosuvastatin restored these levels, suggesting that its protective effects are mediated through the modulation of the NO-Hsp70-WT1 signaling pathway. This study proposes a novel mechanistic framework for statin-mediated vascular protection, highlighting the potential of rosuvastatin to mitigate mechanical stress-induced cardiovascular remodeling in hypertension and related pathologies.

Conclusion

Rosuvastatin can reduce vascular remodeling and allostatic overload during hypertension by decreasing MS-associated apoptosis/fibrosis in mesenteric VSMC and regulating the NO-Hsp70-WT1 axis, which highlights its potential clinical use in treating hypertension-induced vascular remodeling.

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2026-01-15
2026-02-03

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References

  1. Schirone L. Forte M. D’Ambrosio L. An overview of the molecular mechanisms associated with myocardial ischemic injury: State of the art and translational perspectives. Cells 2022 11 7 1165 10.3390/cells11071165 35406729
    [Google Scholar]
  2. Medvedev R.Y. Afolabi S.O. Turner D.G.P. Glukhov A.V. Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis. J. Mol. Cell. Cardiol. 2024 193 11 24 10.1016/j.yjmcc.2024.05.011 38797242
    [Google Scholar]
  3. Zeglinski M.R. Moghadam A.R. Ande S.R. Myocardial cell signaling during the transition to heart failure. Compr. Physiol. 2019 9 1 75 125 10.1002/j.2040‑4603.2019.tb00057.x 30549015
    [Google Scholar]
  4. Umbarkar P. Ejantkar S. Tousif S. Lal H. Mechanisms of fibroblast activation and myocardial fibrosis: Lessons learned from fb-specific conditional mouse models. Cells 2021 10 9 2412 10.3390/cells10092412 34572061
    [Google Scholar]
  5. Mocayar Marón F.J. Ferder L. Saraví F.D. Manucha W. Hypertension linked to allostatic load: From psychosocial stress to inflammation and mitochondrial dysfunction. Stress 2019 22 2 169 181 10.1080/10253890.2018.1542683 30547701
    [Google Scholar]
  6. Stabellini N. Cullen J. Bittencourt M.S. Allostatic load/chronic stress and cardiovascular outcomes in patients diagnosed with breast, lung, or colorectal cancer. J. Am. Heart Assoc. 2024 13 14 033295 10.1161/JAHA.123.033295 38979791
    [Google Scholar]
  7. Tian J.J. Levy M. Zhang X. Sinnott R. Maddela R. Counteracting health risks by Modulating Homeostatic Signaling. Pharmacol. Res. 2022 182 106281 10.1016/j.phrs.2022.106281 35661711
    [Google Scholar]
  8. Sanz R.L. Mazzei L. Manucha W. Implications of the transcription factor WT1 linked to the pathologic cardiac remodeling post-myocardial infarction. Clín. Invest. Arterioscl. 2019 31 3 121 127 10.1016/j.artere.2019.05.002 30292449
    [Google Scholar]
  9. Saheera S. Krishnamurthy P. Cardiovascular changes associated with hypertensive heart disease and aging. Cell Transplant. 2020 29 10.1177/0963689720920830 32393064
    [Google Scholar]
  10. James G.D. Understanding blood pressure variation and variability: Biological importance and clinical significance. Adv. Exp. Med. Biol. 2016 956 3 19 10.1007/5584_2016_83 27722957
    [Google Scholar]
  11. Alexander Y. Osto E. Schmidt-Trucksäss A. Endothelial function in cardiovascular medicine: A consensus paper of the European Society of Cardiology Working Groups on Atherosclerosis and Vascular Biology, Aorta and Peripheral Vascular Diseases, Coronary Pathophysiology and Microcirculation, and Thrombosis. Cardiovasc. Res. 2021 117 1 29 42 10.1093/cvr/cvaa085 32282914
    [Google Scholar]
  12. Shaito A. Aramouni K. Assaf R. Oxidative stress-induced endothelial dysfunction in cardiovascular diseases. Front Biosci Landmark 2022 27 3 105 10.31083/j.fbl2703105 35345337
    [Google Scholar]
  13. Mollace R. Scarano F. Bava I. Modulation of the nitric oxide/cGMP pathway in cardiac contraction and relaxation: Potential role in heart failure treatment. Pharmacol. Res. 2023 196 106931 10.1016/j.phrs.2023.106931 37722519
    [Google Scholar]
  14. Ahmad A. Dempsey S.K. Daneva Z. Role of nitric oxide in the cardiovascular and renal systems. Int. J. Mol. Sci. 2018 19 9 2605 10.3390/ijms19092605 30177600
    [Google Scholar]
  15. He M. Wang D. Xu Y. Nitric oxide-releasing platforms for treating cardiovascular disease. Pharmaceutics 2022 14 7 1345 10.3390/pharmaceutics14071345
    [Google Scholar]
  16. Andrabi S.M. Sharma N.S. Karan A. Nitric oxide: Physiological functions, delivery, and biomedical applications. Adv. Sci. 2023 10 30 2303259 10.1002/advs.202303259 37632708
    [Google Scholar]
  17. Mazzei L. Cuello-Carrión F.D. Docherty N. Manucha W. Heat shock protein 70/nitric oxide effect on stretched tubular epithelial cells linked to WT-1 cytoprotection during neonatal obstructive nephropathy. Int. Urol. Nephrol. 2017 49 10 1875 1892 10.1007/s11255‑017‑1658‑z 28711961
    [Google Scholar]
  18. Mazzei L. Sanz R. Manucha W. Alterations on a key nephrogenic/cardiogenic gene expression linked to hypertension development. Clin. Investig. Arterioscler. 2020 32 2 70 78 10.1016/j.arteri.2019.06.001
    [Google Scholar]
  19. Hastie N.D. Wilms’ tumour 1 (WT1) in development, homeostasis and disease. Development 2017 144 16 2862 2872 10.1242/dev.153163 28811308
    [Google Scholar]
  20. Duim S.N. Goumans M.J. Kruithof B.P.T. WT1 in cardiac development and disease. van den Heuvel-Eibrink MM, Ed. Codon Publications Codon Publications Brisbane, Australia 2016
    [Google Scholar]
  21. Bezdicka M. Kaufman F. Krizova I. Alteration in DNA-binding affinity of Wilms tumor 1 protein due to WT1 genetic variants associated with steroid - resistant nephrotic syndrome in children. Sci. Rep. 2022 12 1 8704 10.1038/s41598‑022‑12760‑x 35610319
    [Google Scholar]
  22. de Oliveira A.A. Priviero F. Webb R.C. Nunes K.P. Impaired HSP70 expression in the aorta of female rats: A novel insight into sex-specific differences in vascular function. Front. Physiol. 2021 12 666696 10.3389/fphys.2021.666696 33967836
    [Google Scholar]
  23. Mazzei L. García M. Calvo J.P. Changes in renal WT-1 expression preceding hypertension development. BMC Nephrol. 2016 17 1 34 10.1186/s12882‑016‑0250‑6 27009470
    [Google Scholar]
  24. Manucha W. Kurbán F. Mazzei L. eNOS/Hsp70 interaction on rosuvastatin cytoprotective effect in neonatal obstructive nephropathy. Eur. J. Pharmacol. 2011 650 2-3 487 495 10.1016/j.ejphar.2010.09.059 20940012
    [Google Scholar]
  25. Mazzei L.J. García I.M. Altamirano L. Docherty N.G. Manucha W. Rosuvastatin preserves renal structure following unilateral ureteric obstruction in the neonatal rat. Am. J. Nephrol. 2012 35 2 103 113 10.1159/000334935 22212364
    [Google Scholar]
  26. García I.M. Mazzei L. Benardón M.E. Caveolin-1–eNOS/Hsp70 interactions mediate rosuvastatin antifibrotic effects in neonatal obstructive nephropathy. Nitric Oxide 2012 27 2 95 105 10.1016/j.niox.2012.05.006 22683596
    [Google Scholar]
  27. Li D.B. Xu H.W. Yang G.J. Yang J.M. Fang H. Tang J.Y. Effects of rosuvastatin correlated with the down-regulation of CYP4A1 in spontaneously hypertensive rats. Microvasc. Res. 2015 98 88 93 10.1016/j.mvr.2015.01.005 25636742
    [Google Scholar]
  28. Zhang Z. Zhang M. Li Y. Simvastatin inhibits the additive activation of ERK1/2 and proliferation of rat vascular smooth muscle cells induced by combined mechanical stress and oxLDL through LOX-1 pathway. Cell. Signal. 2013 25 1 332 340 10.1016/j.cellsig.2012.10.006 23072789
    [Google Scholar]
  29. Natale F. Franzese R. Luisi E. The increasing problem of resistant hypertension: We’ll manage till help comes! Med. Sci. 2024 12 4 53 10.3390/medsci12040053 39449409
    [Google Scholar]
  30. Azevedo P.S. Polegato B.F. Minicucci M.F. Paiva S.A.R. Zornoff L.A.M. Cardiac remodeling: Concepts, clinical impact, pathophysiological mechanisms and pharmacologic treatment. Arq. Bras. Cardiol. 2016 106 1 62 69 10.5935/abc.20160005 26647721
    [Google Scholar]
  31. Alam P. Maliken B.D. Jones S.M. Cardiac remodeling and repair: Recent approaches, advancements, and future perspective. Int. J. Mol. Sci. 2021 22 23 13104 10.3390/ijms222313104 34884909
    [Google Scholar]
  32. Nishida M. Mi X. Ishii Y. Kato Y. Nishimura A. Cardiac remodeling: Novel pathophysiological mechanisms and therapeutic strategies. J. Biochem. 2024 176 4 255 262 10.1093/jb/mvae031 38507681
    [Google Scholar]
  33. Rizzoni D. Agabiti-Rosei C. De Ciuceis C. State of the art review: Vascular remodeling in hypertension. Am. J. Hypertens. 2023 36 1 1 13 10.1093/ajh/hpac093 35961002
    [Google Scholar]
  34. Zeng X. Yang Y. Molecular mechanisms underlying vascular remodeling in hypertension. Rev. Cardiovasc. Med. 2024 25 2 72 10.31083/j.rcm2502072 39077331
    [Google Scholar]
  35. Pang S.C. Venance S.L. Cultured smooth muscle approach in the study of hypertension. Can. J. Physiol. Pharmacol. 1992 70 4 573 579 10.1139/y92‑072 1498722
    [Google Scholar]
  36. Chamley-Campbell J.H. Campbell G.R. Ross R. Phenotype-dependent response of cultured aortic smooth muscle to serum mitogens. J. Cell Biol. 1981 89 2 379 383 10.1083/jcb.89.2.379 7251658
    [Google Scholar]
  37. Pang S.C. Proliferation of aortic smooth muscle cells of genetically hypertensive and normotensive rats in culture. J. Pathol. 1989 158 167 173 10.1002/path.1711580212 2754547
    [Google Scholar]
  38. Griess J.O. On a new series of in which nitrogen is substituted for hydrogen. Philosophical transactions of the Royal Society of London. Series B. Biol Sci 1864 154 667 731
    [Google Scholar]
  39. Susic D. Varagic J. Ahn J. Slama M. Frohlich E.D. Beneficial pleiotropic vascular effects of rosuvastatin in two hypertensive models. J. Am. Coll. Cardiol. 2003 42 6 1091 1097 10.1016/S0735‑1097(03)00926‑4 13678936
    [Google Scholar]
  40. Ott C. Schlaich M.P. Schmidt B.M.W. Titze S.I. Schäufele T. Schmieder R.E. Rosuvastatin improves basal nitric oxide activity of the renal vasculature in patients with hypercholesterolemia. Atherosclerosis 2008 196 2 704 711 10.1016/j.atherosclerosis.2006.12.020 17298834
    [Google Scholar]
  41. Nangle M.R. Cotter M.A. Cameron N.E. Effects of rosuvastatin on nitric oxide-dependent function in aorta and corpus cavernosum of diabetic mice: Relationship to cholesterol biosynthesis pathway inhibition and lipid lowering. Diabetes 2003 52 9 2396 2402 10.2337/diabetes.52.9.2396 12941781
    [Google Scholar]
  42. Pelat M. Dessy C. Massion P. Desager J.P. Feron O. Balligand J.L. Rosuvastatin decreases caveolin-1 and improves nitric oxide-dependent heart rate and blood pressure variability in apolipoprotein E-/- mice in vivo. Circulation 2003 107 19 2480 2486 10.1161/01.CIR.0000065601.83526.3E 12719275
    [Google Scholar]
  43. Gorabi A. Kiaie N. Hajighasemi S. Statin-induced nitric oxide signaling: Mechanisms and therapeutic implications. J. Clin. Med. 2019 8 12 2051 10.3390/jcm8122051 31766595
    [Google Scholar]
  44. Saad H.M. Elekhnawy E. Shaldam M.A. Rosuvastatin and diosmetin inhibited the HSP70/TLR4/NF-κB p65/NLRP3 signaling pathways and switched macrophage to M2 phenotype in a rat model of acute kidney injury induced by cisplatin. Biomed. Pharmacother. 2024 171 116151 10.1016/j.biopha.2024.116151 38262148
    [Google Scholar]
  45. Dinapoli P. Taccardi A. Grilli A. Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia–reperfusion injury in rat hearts. Cardiovasc. Res. 2005 66 3 462 471 10.1016/j.cardiores.2005.02.008 15914111
    [Google Scholar]
  46. Huang B. Li F.A. Wu C.H. Wang D.L. The role of nitric oxide on rosuvastatin-mediated S-nitrosylation and translational proteomes in human umbilical vein endothelial cells. Proteome Sci. 2012 10 1 43 10.1186/1477‑5956‑10‑43 22799578
    [Google Scholar]
  47. Xu J.Z. Chai Y.L. Zhang Y.L. Effect of rosuvastatin on high glucose-induced endoplasmic reticulum stress in human umbilical vein endothelial cells. Genet. Mol. Res. 2016 15 4 10.4238/gmr15048935 27813604
    [Google Scholar]
  48. Feng P.F. Zhang B. Zhao L. Intracellular mechanism of rosuvastatin-induced decrease in mature herg protein expression on membrane. Mol. Pharm. 2019 16 4 1477 1488 10.1021/acs.molpharmaceut.8b01102 30807184
    [Google Scholar]
  49. Kata D. Földesi I. Feher L.Z. Hackler L. Puskas L.G. Gulya K. Rosuvastatin enhances anti-inflammatory and inhibits pro-inflammatory functions in cultured microglial cells. Neuroscience 2016 314 47 63 10.1016/j.neuroscience.2015.11.053 26633263
    [Google Scholar]
  50. Shakirova V. Markelova M. Davidyuk Y. Rosuvastatin as a supplemental treatment for the clinical symptoms of nephropathia epidemica: A pilot clinical study. Viruses 2024 16 2 306 10.3390/v16020306 38400081
    [Google Scholar]
  51. Mazzei L. García I.M. Cacciamani V. Benardón M.E. Manucha W. WT-1 mRNA expression is modulated by nitric oxide availability and Hsp70 interaction after neonatal unilateral ureteral obstruction. Biocell 2010 34 3 121 132 21443142
    [Google Scholar]
  52. Tomek J. Bub G. Hypertension‐induced remodelling: On the interactions of cardiac risk factors. J. Physiol. 2017 595 12 4027 4036 10.1113/JP273043 28217927
    [Google Scholar]
  53. Renna N.F. de las Heras N. Miatello R.M. Pathophysiology of vascular remodeling in hypertension. Int. J. Hypertens. 2013 2013 1 7 10.1155/2013/808353 23970958
    [Google Scholar]
  54. Huang X. Hu L. Long Z. Wang X. Wu J. Cai J. Hypertensive heart disease: Mechanisms, diagnosis and treatment. Rev. Cardiovasc. Med. 2024 25 3 93 10.31083/j.rcm2503093 39076964
    [Google Scholar]
  55. Snelders M. Yildirim M. Danser A.H.J. van der Pluijm I. Essers J. The extracellular matrix and cardiac pressure overload: Focus on novel treatment targets. Cells 2024 13 20 1685 10.3390/cells13201685 39451203
    [Google Scholar]
  56. Humphrey J.D. Mechanisms of vascular remodeling in hypertension. Am. J. Hypertens. 2021 34 5 432 441 10.1093/ajh/hpaa195 33245319
    [Google Scholar]
  57. Brown I.A.M. Diederich L. Good M.E. Vascular smooth muscle remodeling in conductive and resistance arteries in hypertension. Arterioscler. Thromb. Vasc. Biol. 2018 38 9 1969 1985 10.1161/ATVBAHA.118.311229 30354262
    [Google Scholar]
  58. Zhao J. Yoshizumi M. A comprehensive retrospective study on the mechanisms of cyclic mechanical stretch-induced vascular smooth muscle cell death underlying aortic dissection and potential therapeutics for preventing acute aortic aneurysm and associated ruptures. Int. J. Mol. Sci. 2024 25 5 2544 10.3390/ijms25052544 38473793
    [Google Scholar]
  59. Lv Q. Wang Y. Li Y. Rosuvastatin reverses hypertension-induced changes in the aorta structure and endothelium-dependent relaxation in rats through suppression of apoptosis and inflammation. J. Cardiovasc. Pharmacol. 2020 75 6 584 595 10.1097/FJC.0000000000000828 32205566
    [Google Scholar]
  60. Bruder-Nascimento T. Callera G.E. Montezano A.C. Belin de Chantemele E.J. Tostes R.C. Touyz R.M. Atorvastatin inhibits pro-inflammatory actions of aldosterone in vascular smooth muscle cells by reducing oxidative stress. Life Sci. 2019 221 221 29 34 10.1016/j.lfs.2019.01.043 30721707
    [Google Scholar]
  61. Chen W.H. Chen C.H. Hsu M.C. Chang R.W. Wang C.H. Lee T.S. Advances in the molecular mechanisms of statins in regulating endothelial nitric oxide bioavailability: Interlocking biology between eNOS activity and L-arginine metabolism. Biomed. Pharmacother. 2024 171 116192 10.1016/j.biopha.2024.116192 38262153
    [Google Scholar]
  62. Jufri N.F. Mohamedali A. Avolio A. Baker M.S. Mechanical stretch: Physiological and pathological implications for human vascular endothelial cells. Vasc. Cell 2015 7 1 8 10.1186/s13221‑015‑0033‑z 26388991
    [Google Scholar]
  63. Luo S.S. Sugimoto K. Fujii S. Takemasa T. Fu S.B. Yamashita K. Role of heat shock protein 70 in induction of stress fiber formation in rat arterial endothelial cells in response to stretch stress. Acta Histochem. Cytochem. 2007 40 1 9 17 10.1267/ahc.06011 17375204
    [Google Scholar]
  64. Xu Q. Schett G. Li C. Hu Y. Wick G. Mechanical stress-induced heat shock protein 70 expression in vascular smooth muscle cells is regulated by Rac and Ras small G proteins but not mitogen-activated protein kinases. Circ. Res. 2000 86 11 1122 1128 10.1161/01.RES.86.11.1122 10850962
    [Google Scholar]
  65. Duim S.N. Kurakula K. Goumans M.J. Kruithof B.P.T. Cardiac endothelial cells express Wilms’ tumor-1. J. Mol. Cell. Cardiol. 2015 81 127 135 10.1016/j.yjmcc.2015.02.007 25681586
    [Google Scholar]
  66. Alidadi M. Montecucco F. Jamialahmadi T. Al-Rasadi K. Johnston T.P. Sahebkar A. Beneficial effect of statin therapy on arterial stiffness. BioMed Res. Int. 2021 2021 1 5548310 10.1155/2021/5548310 33860033
    [Google Scholar]
  67. Mangione C.M. Barry M.J. Nicholson W.K. Statin use for the primary prevention of cardiovascular disease in adults. JAMA 2022 328 8 746 753 10.1001/jama.2022.13044 35997723
    [Google Scholar]
  68. Heiston E.M. Hundley W.G. Statins for cardiac and vascular protection during and after cancer therapy. Curr. Oncol. Rep. 2022 24 5 555 561 10.1007/s11912‑022‑01212‑4 35199294
    [Google Scholar]
  69. Fan C.H. Hao Y. Liu Y.H. Anti-inflammatory effects of rosuvastatin treatment on coronary artery ectasia patients of different age groups. BMC Cardiovasc. Disord. 2020 20 1 330 10.1186/s12872‑020‑01604‑z 32652935
    [Google Scholar]
  70. Mahalwar R. Khanna D. Pleiotropic antioxidant potential of rosuvastatin in preventing cardiovascular disorders. Eur. J. Pharmacol. 2013 711 1-3 57 62 10.1016/j.ejphar.2013.04.025 23648561
    [Google Scholar]
  71. Yang L. Li X. Ni L. Lin Y. Treatment of endothelial cell dysfunction in atherosclerosis: A new perspective integrating traditional and modern approaches. Front. Physiol. 2025 16 1555118 10.3389/fphys.2025.1555118 40206381
    [Google Scholar]
  72. Widlansky M.E. Gokce N. Keaney J.F. Vita J.A. The clinical implications of endothelial dysfunction. J. Am. Coll. Cardiol. 2003 42 7 1149 1160 10.1016/S0735‑1097(03)00994‑X 14522472
    [Google Scholar]
  73. Steger-Hartmann T. Raschke M. Translating in vitro to in vivo and animal to human. Curr. Opin. Toxicol. 2020 23-24 6 10 10.1016/j.cotox.2020.02.003
    [Google Scholar]
  74. Mattes W.B. In vitro to in vivo translation. Curr. Opin. Toxicol. 2020 23-24 114 118 10.1016/j.cotox.2020.09.001
    [Google Scholar]
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Rosuvastatin Reduces Allostatic Overload due to Mechanical Strain: A New Finding on Vascular Remodeling Linked to Hypertension in Spontaneously Hypertensive Rats
Bentham Science Publishers ; https://doi.org/10.2174/0115734021400864251020044405
/content/journals/chyr/10.2174/0115734021400864251020044405
/content/journals/chyr/10.2174/0115734021400864251020044405
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  • Article Type:     Research Article
Keywords: heat shock protein 70 ; rosuvastatin ; Hypertension ; mechanical stretch ; nitric oxide ; Wilms tumor protein 1

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